[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 27 of about 27
1. Chang HK, Kim JH: Classical malignant rhabdoid tumor of central nervous system in 9-year-old Korean. Yonsei Med J; 2001 Feb;42(1):142-6
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Classical malignant rhabdoid tumor of central nervous system in 9-year-old Korean.
  • A Malignant rhabdoid tumor (MRT) arising in the right temporoparietal lobe of a 9-year-old boy is described along with the results of an immunohistochemical study.
  • The child underwent a subtotal resection of the tumor, followed by radiotherapy and systemic chemotherapy, but died three years after surgery.
  • A MRT, a primary neoplasm of the central nervous system (CNS), is an entity of unknown histogenesis with a dismal prognosis, which only occurs in early childhood.
  • Histologically similar tumors with more varied morphological features have been designated as an atypical teratoid/rhabdoid tumor.
  • However, a classical MRT is extremely rare in the CNS and our case represents a classical CNS MRT.
  • [MeSH-major] Brain Neoplasms / metabolism. Rhabdoid Tumor / metabolism

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11293495.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Vimentin
  •  go-up   go-down


2. Pollack IF, Boyett JM, Yates AJ, Burger PC, Gilles FH, Davis RL, Finlay JL, Children's Cancer Group: The influence of central review on outcome associations in childhood malignant gliomas: results from the CCG-945 experience. Neuro Oncol; 2003 07;5(3):197-207
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The influence of central review on outcome associations in childhood malignant gliomas: results from the CCG-945 experience.
  • To examine the influence of the pathology review mechanism on the results of analyses of therapeutic efficacy and biological prognostic correlates for pediatric high-grade gliomas, we evaluated the effects of using single-expert review or consensus review, as alternatives to institutional classification, in determining outcome results of a large randomized trial.
  • The study group was the randomized cohort of Children's Cancer Group study 945, which compared efficacy of 2 chemotherapy regimens adjuvant to surgery and radiation.
  • Sections of study tumors also were centrally reviewed, initially by a study review neuropathologist and subsequently by 5 neuropathologists, including the review pathologist.
  • Among 172 eligible patients, 42 tumors were classified as discordant on single-expert review and 51 on consensus review.
  • Progression-free survival probabilities calculated for patients with tumors classified as high-grade gliomas by either single-expert or consensus review were inferior to those for the overall, institutionally diagnosed cohort.
  • However, conclusions of the study regarding relative efficacy of treatment and clinical and molecular outcome correlates were unaffected by diagnosis method.
  • However, comparisons between arms in which inclusion was determined by different review criteria for each arm caused spurious conclusions about efficacy differences between treatments.
  • We conclude that the pathology review mechanism had little effect on within-trial comparisons of therapeutic effects or prognostic correlates in this randomized study, but strongly influenced survival distributions that were calculated for each treatment arm.
  • These results support the implementation of expedited central review in therapeutic studies involving childhood malignant gliomas as a way to prospectively identify and exclude cases with discordant diagnoses and indicate the need for additional measures, such as molecular assessments, to increase the reproducibility of neuropathologic classification for these tumors.
  • [MeSH-major] Antineoplastic Protocols / standards. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / therapy. Glioma / pathology. Glioma / therapy
  • [MeSH-minor] Child. Combined Modality Therapy / methods. Combined Modality Therapy / statistics & numerical data. Confidence Intervals. Humans. Prospective Studies. Randomized Controlled Trials as Topic. Retrospective Studies. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12816726.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 21765; United States / NINDS NIH HHS / NS / NS 37704
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1920685
  •  go-up   go-down


3. Frühwald MC, Rickert CH, O'Dorisio MS, Madsen M, Warmuth-Metz M, Khanna G, Paulus W, Kühl J, Jürgens H, Schneider P, Müller HL: Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging. Clin Cancer Res; 2004 May 1;10(9):2997-3006
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatostatin receptor subtype 2 is expressed by supratentorial primitive neuroectodermal tumors of childhood and can be targeted for somatostatin receptor imaging.
  • PURPOSE: Although gliomas predominate among central nervous system (CNS) neoplasms in adulthood, embryonal tumors are the most common malignant brain tumors in children.
  • Despite novel treatment approaches, including improved radiotherapy and high-dose chemotherapy, survival rates remain unsatisfactory.
  • The timely diagnosis of residual or recurrent embryonal CNS tumors and thus the earliest possible time point for intervention is often hampered by inaccuracies of conventional imaging techniques.
  • Here, we evaluated somatostatin receptor type 2 (sst(2)) expression using an antibody in an array of CNS tumors of childhood.
  • Eight high-grade gliomas, 4 atypical teratoid/rhabdoid tumors, 7 supratentorial primitive neuroectodermal tumors (stPNET), 1 medulloepithelioma (ME), and 8 ependymomas were screened.
  • Tumors positive in vitro were additionally analyzed in vivo using SRI.
  • RESULTS: Abundant expression of somatostatin receptor type 2 in stPNET, a ME, and ependymomas warranted in vivo imaging of 7 stPNET, 1 rhabdomyosarcoma, 3 ependymomas, 1 ME, and 1 glioblastoma.
  • In selected cases SRI was more sensitive in the detection of relapse than conventional imaging by magnetic resonance imaging and computed tomography.
  • CONCLUSIONS: SRI should be considered in the evaluation of residual or recurrent embryonal CNS tumors, especially stPNET.
  • The strengths of SRI lie in the differentiation of reactive tissue changes versus residual or recurrent tumor, the detection of small lesions, and possibly in the distinction of stPNET from gliomas.
  • [MeSH-major] Neuroectodermal Tumors, Primitive / pathology. Receptors, Somatostatin / biosynthesis. Supratentorial Neoplasms / pathology
  • [MeSH-minor] Central Nervous System Neoplasms / metabolism. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / radionuclide imaging. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Infant. Male. Tomography, Emission-Computed, Single-Photon / methods

  • Genetic Alliance. consumer health - Supratentorial primitive neuroectodermal tumors, childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15131035.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2
  •  go-up   go-down


Advertisement
4. Löning L, Zimmermann M, Reiter A, Kaatsch P, Henze G, Riehm H, Schrappe M: Secondary neoplasms subsequent to Berlin-Frankfurt-Münster therapy of acute lymphoblastic leukemia in childhood: significantly lower risk without cranial radiotherapy. Blood; 2000 May 1;95(9):2770-5
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary neoplasms subsequent to Berlin-Frankfurt-Münster therapy of acute lymphoblastic leukemia in childhood: significantly lower risk without cranial radiotherapy.
  • Secondary neoplasms (SNs) represent serious late complications after successful treatment of malignant diseases.
  • To evaluate the rate and type of SNs after Berlin-Frankfurt-Münster (BFM) treatment in children with acute lymphoblastic leukemia (ALL), we analyzed the data from the BFM database and the German Childhood Cancer Registry (GCCR).
  • The median follow-up time from diagnosis was 5.7 years (range 1.5-18 years).
  • By December 1997, 52 SNs were documented, including 16 acute myeloid leukemias (AMLs), 13 neoplasms of the central nervous system (CNS), and 23 other neoplasms.
  • Compared with the expected numbers estimated from incidence rates derived from the GCCR, this represented a 14-fold increase for all cancers and a 19-fold increase for CNS tumors.
  • SNs developed 0.9 to 15 years (median: 6 years) after the diagnosis of ALL; 46 patients were in first complete remission (CR).
  • 5%) after treatment, including cranial irradiation and significantly lower in nonirradiated patients: 1.2% (95% CI: 0.2%-2.3%; P =.048).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Brain Neoplasms / prevention & control. Brain Neoplasms / secondary. Child. Child, Preschool. Combined Modality Therapy. Databases as Topic. Disease-Free Survival. Female. Follow-Up Studies. Germany. Humans. Infant. Infant, Newborn. Male. Registries. Retrospective Studies. Risk Factors. Survival Analysis

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10779419.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  •  go-up   go-down


5. Rodini CO, Suzuki DE, Nakahata AM, Pereira MC, Janjoppi L, Toledo SR, Okamoto OK: Aberrant signaling pathways in medulloblastomas: a stem cell connection. Arq Neuropsiquiatr; 2010 Dec;68(6):947-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Medulloblastoma is a highly malignant primary tumor of the central nervous system.
  • It represents the most frequent type of solid tumor and the leading cause of death related to cancer in early childhood.
  • Current treatment includes surgery, chemotherapy and radiotherapy which may lead to severe cognitive impairment and secondary brain tumors.
  • New perspectives for therapeutic development have emerged with the identification of stem-like cells displaying high tumorigenic potential and increased radio- and chemo-resistance in gliomas.
  • From the clinical viewpoint, modulation of signaling pathways such as TGFβ, regulating neural stem cell proliferation and tumor development, might be attempted as an alternative strategy for future drug development aiming at more efficient therapies and improved clinical outcome of patients with pediatric brain cancers.
  • [MeSH-major] Cerebellar Neoplasms / pathology. Medulloblastoma / pathology. Neoplastic Stem Cells / pathology. Neural Stem Cells / pathology. Signal Transduction. Transforming Growth Factor beta

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21243257.001).
  • [ISSN] 1678-4227
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta
  •  go-up   go-down


6. Rossi A, Caracciolo V, Russo G, Reiss K, Giordano A: Medulloblastoma: from molecular pathology to therapy. Clin Cancer Res; 2008 Feb 15;14(4):971-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medulloblastoma: from molecular pathology to therapy.
  • Medulloblastoma is the most common malignant tumor of central nervous system in children.
  • Currently, multimodality treatment, including surgery, radiotherapy, and chemotherapy is considered as the most effective strategy against these malignant cerebellar tumors of the childhood.
  • Attempts to further reduce the morbidity and mortality associated with medulloblastoma have been restricted by the toxicity of conventional treatments and the infiltrative nature of the disease.
  • Over the past decade, new discoveries in molecular biology have revealed new insights in signaling pathways regulating medulloblastoma tumor formation.
  • Recent advances in the molecular biology of medulloblastoma indicate that the classification of these embryonal tumors, solely based on histology and clinical criteria, may not be adequate enough.
  • Better understanding of the growth control mechanisms involved in the development and progression of medulloblastoma will allow a better classification, leading to the improvement of the existing therapies, as well as to the development of new therapeutic approaches.

  • Genetic Alliance. consumer health - Medulloblastoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1996 Jan 15;56(2):377-83 [8542595.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jan;50(1):163-6 [16724315.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2085-8 [9187099.001]
  • [Cites] Cancer Res. 1999 Feb 1;59(3):711-9 [9973222.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):832-45 [10071274.001]
  • [Cites] Int J Clin Oncol. 2004 Dec;9(6):471-4 [15616877.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):978-86 [15758008.001]
  • [Cites] Oncogene. 2005 Jun 2;24(24):3923-31 [15806170.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):4975-8 [15958535.001]
  • [Cites] Nature. 2005 Jun 16;435(7044):903-10 [15959507.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4215-22 [16618744.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 Sep;58(3):343-7 [16408203.001]
  • [Cites] J Clin Oncol. 1999 Jul;17(7):2127-36 [10561268.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Jan 15;46(2):269-79 [10661332.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):383-9 [10667591.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):433-7 [10666372.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):77-81 [10738305.001]
  • [Cites] Genes Dev. 2000 Apr 15;14(8):994-1004 [10783170.001]
  • [Cites] Nat Med. 2000 Jul;6(7):826-31 [10888935.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(16):3004-11 [10944134.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(23):9055-67 [11074003.001]
  • [Cites] J Clin Oncol. 2001 May 15;19(10):2696-704 [11352962.001]
  • [Cites] Mol Pathol. 2001 Oct;54(5):331-7 [11577176.001]
  • [Cites] Nat Genet. 2001 Oct;29(2):143-52 [11544480.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5897-905 [12185589.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] Int J Cancer. 2002 Sep 10;101(2):198-201 [12209999.001]
  • [Cites] Genes Dev. 2002 Nov 1;16(21):2743-8 [12414725.001]
  • [Cites] Development. 2003 Jan;130(1):15-28 [12441288.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):140-8 [12517790.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1581-91 [12697884.001]
  • [Cites] Pediatr Neurosurg. 2003 Dec;39(6):299-304 [14734863.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):984-93 [14970185.001]
  • [Cites] Lancet Oncol. 2004 Apr;5(4):209-18 [15050952.001]
  • [Cites] Neoplasia. 2004 Jul-Aug;6(4):310-22 [15256053.001]
  • [Cites] J Neurosurg. 1994 Nov;81(5):690-8 [7931615.001]
  • [Cites] J Neurooncol. 1994;19(2):169-73 [7964993.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5220-7 [16936740.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5263-7 [16936746.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5294-301 [16936750.001]
  • [Cites] Oncogene. 2006 Aug 28;25(38):5333-40 [16936755.001]
  • [Cites] J Clin Oncol. 2006 Sep 1;24(25):4202-8 [16943538.001]
  • [Cites] Lancet Oncol. 2006 Oct;7(10):813-20 [17012043.001]
  • [Cites] J Cell Physiol. 2007 Jan;210(1):183-91 [16998811.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):3004-14 [16956759.001]
  • [Cites] Indian J Pathol Microbiol. 2006 Oct;49(4):535-9 [17183845.001]
  • [Cites] Lab Invest. 2007 Feb;87(2):97-103 [17211410.001]
  • [Cites] Nat Clin Pract Oncol. 2007 May;4(5):295-304 [17464337.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1814-23 [9164190.001]
  • (PMID = 18281528.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095518-08; United States / NCI NIH HHS / CA / R01 CA095518; United States / NCI NIH HHS / CA / R01 CA095518-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 50
  • [Other-IDs] NLM/ NIHMS279562; NLM/ PMC3222918
  •  go-up   go-down


7. Badruddoja MA, Keir ST, King I, Zeidner J, Vredenburgh JJ, Muhlbaier LH, Bigner DD, Friedman HS: Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice. Neuro Oncol; 2007 Jul;9(3):240-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of VNP40101M (Cloretazine) in the treatment of CNS tumor xenografts in athymic mice.
  • The current study was designed to assess the activity of VNP40101M administered at a dose of 18 mg/kg daily for five days against a panel of human adult and pediatric CNS tumors growing subcutaneously or intracranially in athymic nude mice.
  • The results demonstrated statistically significant (p < 0.05) growth delays of 15.0, 8.3, 51.0, 60+, 60+, and 60+ days in subcutaneous xenografts derived from childhood glioblastoma multiforme (D-456 MG), childhood ependymoma (D-528 EP and D-612 EP), childhood medulloblastoma (D-425 MED), and adult malignant glioma (D-245 MG and D-54 MG), respectively, with corresponding tumor regressions in 10 of 10, 4 of 10, 8 of 10, 9 of 10, 9 of 10, and 10 of 10 treated mice, respectively.
  • Delayed toxicity was seen more than 60 days after treatment, with 23 deaths in 100 treated animals, despite a median weight loss of only 0.06%.
  • In mice bearing intracranial D-245 MG xenografts, treatment with VNP40101M at a dose of 18 mg/kg daily for five days produced a 50% increase in median survival compared with controls.
  • Additional experiments conducted against subcutaneous D-245 MG xenografts by using reduced doses of 13.5 or 9.0 mg/kg daily for five days demonstrated tumor growth delays of 82.2 and 53.5 days, with corresponding tumor regressions in 8 of 9 and 9 of 10 treated mice, respectively (all values, p < 0.001), with one toxic death.
  • These findings suggest that VNP40101M is active in the treatment of a wide range of human central nervous system tumors and warrants translation to the clinic.

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Chemother Pharmacol. 1994;34(2):171-4 [8194169.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2933-6 [9230204.001]
  • [Cites] Invest New Drugs. 2005 Mar;23(2):123-35 [15744588.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009.001]
  • [Cites] Biochem Pharmacol. 2000 Feb 1;59(3):283-91 [10609557.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3033-8 [11306484.001]
  • [Cites] Int J Toxicol. 2002 Jan-Feb;21(1):23-38 [11936896.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):288-95 [14685775.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2908-17 [15131024.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Neurosurgery. 1979 Apr;4(4):308-14 [450229.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4189-95 [3390813.001]
  • [Cites] J Neurooncol. 1994;20(2):111-20 [7807189.001]
  • (PMID = 17522334.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P50 NS020023; United States / NINDS NIH HHS / NS / 5P50-NS20023-23
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Prodrugs; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
  • [Other-IDs] NLM/ PMC1907418
  •  go-up   go-down


8. Daly BP, Brown RT: Scholarly literature review: management of neurocognitive late effects with stimulant medication. J Pediatr Psychol; 2007 Oct;32(9):1111-26
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scholarly literature review: management of neurocognitive late effects with stimulant medication.
  • OBJECTIVE: To examine the extant literature on stimulant drug therapy for survivors of childhood cancer during the late-effects period.
  • METHODS: A review of literature is provided on the mechanism of and cognitive toxicities for children and adolescents treated for acute lymphoblastic leukemia (ALL) and malignant brain tumors (BT) as well as the pharmacotherapy of stimulant medications, with a specific review of literature on the efficacy and safety of the stimulants for children with ALL and BT.
  • RESULTS: Only four studies were found that have examined the effects of stimulant medication on the cognitive toxicities of childhood survivors of cancer during the late-effects period and only two of these investigations were controlled clinical trials.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / psychology. Central Nervous System Stimulants / pharmacology. Central Nervous System Stimulants / therapeutic use. Cognition / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17442692.001).
  • [ISSN] 0146-8693
  • [Journal-full-title] Journal of pediatric psychology
  • [ISO-abbreviation] J Pediatr Psychol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants
  • [Number-of-references] 150
  •  go-up   go-down


9. Marachelian A, Butturini A, Finlay J: Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue for childhood central nervous system tumors. Bone Marrow Transplant; 2008 Jan;41(2):167-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue for childhood central nervous system tumors.
  • Myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue has been evaluated in the treatment of children and young adults with brain tumors for whom conventional therapy is either too toxic (for example, radiotherapy in infants) or ineffective (for example, recurrent malignant tumors).
  • With this strategy, myeloablative chemotherapy is administered to patients after initial surgery, and standard-dose chemotherapy.
  • The success of myeloablative chemotherapy depends on the histological type of tumor, extent of disease and of surgical resection, and response to prior chemotherapy.
  • Here, we review results of myeloablative chemotherapy with hematopoietic progenitor cell rescue in brain tumors of different histologies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy / methods. Disease-Free Survival. Humans. Myeloablative Agonists / therapeutic use. Transplantation Conditioning. Transplantation, Autologous / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18176620.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  • [Number-of-references] 47
  •  go-up   go-down


10. Bouhoula A, Boubaker A, Kallel J, Chikili R, Kchir N, Khaldi M: [Central nervous system medulloepithelioma. A report of three cases]. Neurochirurgie; 2010 Oct;56(5):395-400

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Central nervous system medulloepithelioma. A report of three cases].
  • [Transliterated title] Le médulloépithéliome du système nerveux central. À propos de trois cas.
  • Central nervous system medulloepithelioma is a rare, highly malignant childhood tumor.
  • It might be confused with medulloblastoma or other primitive neuroectodermal tumors, but it is quite particular by its clinical, radiological, and pathological features.
  • Only two reported cases in the literature survived beyond 4 years after treatment by gross total resection and radiotherapy without chemotherapy.
  • Two patients underwent a gross-total resection followed by radiotherapy and survived more than 4 years after treatment.
  • The third case had, however, recurred twice within the 1st postoperative month despite a complete resection each time and metastasis to the lung developed.
  • Chemotherapy was then carried out after the third procedure and the patient died 7 months later.
  • [MeSH-major] Neuroectodermal Tumors, Primitive. Supratentorial Neoplasms

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20708758.001).
  • [ISSN] 1773-0619
  • [Journal-full-title] Neuro-Chirurgie
  • [ISO-abbreviation] Neurochirurgie
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


11. Witt TC, Lo SS, Timmerman RD: Successful treatment of a skull base malignant rhabdoid tumor with surgery, chemotherapy and gamma Knife-based stereotactic radiosurgery in a young child. Stereotact Funct Neurosurg; 2007;85(6):310-3
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of a skull base malignant rhabdoid tumor with surgery, chemotherapy and gamma Knife-based stereotactic radiosurgery in a young child.
  • Most childhood rhabdoid tumors occur in the kidney or central nervous system but they can occur in other sites and they usually run an aggressive clinical course.
  • We report a case of an 8-month-old boy with a right temporal bone rhabdoid tumor treated with surgery, chemotherapy and Gamma Knife-based stereotactic radiosurgery.
  • Gamma Knife-based stereotactic radiosurgery may have a role in the management of very young children with skull base tumors.
  • [MeSH-major] Radiosurgery. Rhabdoid Tumor / drug therapy. Rhabdoid Tumor / surgery. Skull Base Neoplasms / drug therapy. Skull Base Neoplasms / surgery
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Humans. Infant. Magnetic Resonance Imaging. Male. Stereotaxic Techniques / instrumentation

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • [ErratumIn] Stereotact Funct Neurosurg. 2010;88(6):389
  • (PMID = 17709987.001).
  • [ISSN] 1423-0372
  • [Journal-full-title] Stereotactic and functional neurosurgery
  • [ISO-abbreviation] Stereotact Funct Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


12. Sklar CA: Childhood brain tumors. J Pediatr Endocrinol Metab; 2002 May;15 Suppl 2:669-73
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Childhood brain tumors.
  • Primary malignant tumors of the central nervous system (CNS) account for about 16% of all childhood malignancies.
  • These tumors are the second most common type of childhood cancer and the most frequent of the solid tumors.
  • CNS tumors are diverse, representing many histological types and arising in a variety of anatomic sites.
  • The most common malignant tumors include astrocytomas (52%), medulloblastomas/primitive neuroectodermal tumors (PNETs) (21%), gliomas (19%), and ependymomas (9%).
  • The current 5-year survival rate for all pediatric CNS tumors is 67%, but rates differ considerably among tumor types.
  • Treatment modalities also differ according to histological type.
  • Currently, about 25% of patients are treated with surgery alone, 40% undergo surgery plus radiation, and 30% are treated with surgery, radiation, and chemotherapy.
  • Survivors of childhood brain tumors are at substantial risk for increased morbidity and late mortality.
  • Five-year survivors of brain tumors are 13 times more likely to die than healthy age- and sex-matched peers.
  • Neurological, neurocognitive, and endocrine disturbances are the most prevalent disabilities observed among long-term survivors of pediatric brain tumors.
  • [MeSH-major] Brain Neoplasms / epidemiology
  • [MeSH-minor] Child. Humans. Hypothalamus / pathology. Pituitary Neoplasms / pathology. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12092679.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 20
  •  go-up   go-down


13. Zimmerman MA, Goumnerova LC, Proctor M, Scott RM, Marcus K, Pomeroy SL, Turner CD, Chi SN, Chordas C, Kieran MW: Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor. J Neurooncol; 2005 Mar;72(1):77-84
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor.
  • Atypical teratoid/rhabdoid tumors (AT/RT) are highly malignant lesions of childhood that carry a very poor prognosis.
  • AT/RT can occur in the central nervous system (CNS AT/RT) and disease in this location carries an even worse prognosis with a median survival of 7 months.
  • In spite of multiple treatment regimens consisting of maximal surgical resection (including second look surgery), radiation therapy (focal and craniospinal), and multi-agent intravenous, oral and intrathecal chemotherapy, with or without high-dose therapy and stem cell rescue, only seven long-term survivors of CNS AT/RT have been reported, all in patients with newly diagnosed disease.
  • For this reason, many centers now direct such patients, particularly those under 5 years of age, or those with recurrent disease, towards comfort care rather than attempt curative therapy.
  • We now report on four children, two with newly diagnosed CNS AT/RT and two with progressive disease after multi-agent chemotherapy who are long term survivors (median follow-up of 37 months) using a combination of surgery, radiation therapy, and intensive chemotherapy.
  • The chemotherapy component was modified from the Intergroup Rhabdomyosarcoma Study Group (IRS III) parameningeal protocol as three of the seven reported survivors in the literature were treated using this type of therapy.
  • Our four patients, when added to the three reported survivors in the literature using this approach, suggest that patients provided this aggressive therapy can significantly alter the course of their disease.
  • More importantly, we report on the first two survivors after relapse with multi-agent intravenous and intrathecal chemotherapy treated with this modified regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Neoplasm Recurrence, Local / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant / methods. Child. Child, Preschool. Female. Humans. Infant. Male. Radiotherapy, Adjuvant / methods. Remission Induction. Survival Analysis

  • Genetic Alliance. consumer health - Rhabdoid tumor.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;412(4):393-7 [3125680.001]
  • [Cites] Childs Nerv Syst. 1993 Jun;9(3):185-90; discussion 190 [8397069.001]
  • [Cites] J Neurooncol. 2001 Mar;52(1):49-56 [11451202.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):121-6 [12622450.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jul 15;41(5):1013-9 [9719110.001]
  • [Cites] Genes Chromosomes Cancer. 2000 May;28(1):31-7 [10738300.001]
  • [Cites] Arch Ophthalmol. 1967 Dec;78(6):709-13 [4294312.001]
  • [Cites] Surg Neurol. 1992 May;37(5):410-4 [1631771.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):37-40 [7459813.001]
  • [Cites] J Neurooncol. 1995;24(1):21-8 [8523069.001]
  • [Cites] Childs Nerv Syst. 1997 Jul;13(7):418-21 [9298280.001]
  • [Cites] Surv Ophthalmol. 1994 Jan-Feb;38(4):365-70 [8160109.001]
  • [Cites] Neuroradiology. 2000 May;42(5):363-7 [10872158.001]
  • [Cites] Semin Diagn Pathol. 1986 May;3(2):151-63 [3616219.001]
  • [Cites] J Neurooncol. 1999 May;43(1):63-70 [10448873.001]
  • [Cites] Med Pediatr Oncol. 1991;19(4):310-7 [2056976.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):710-4 [2213160.001]
  • [Cites] Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1989 Sep-Oct;30(5):316-22 [2484056.001]
  • [Cites] Acta Neuropathol. 1992;83(4):445-8 [1575023.001]
  • [Cites] J Neurooncol. 2000 May;48(1):41-5 [11026695.001]
  • [Cites] Can J Neurol Sci. 1994 Aug;21(3):273-7 [8000986.001]
  • [Cites] AJNR Am J Neuroradiol. 1993 Jan-Feb;14 (1):107-15 [8427070.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Jun-Jul;24(5):337-42 [12142780.001]
  • [Cites] Surg Neurol. 1993 Nov;40(5):429-34 [8211663.001]
  • [Cites] Neuropathol Appl Neurobiol. 2003 Jun;29(3):254-61 [12787322.001]
  • [Cites] J Neurooncol. 1998 Dec;40(3):265-75 [10066100.001]
  • [Cites] J Neurooncol. 1995;25(3):193-203 [8592169.001]
  • [Cites] AJNR Am J Neuroradiol. 1995 Sep;16(8):1727-8 [7502982.001]
  • [Cites] Pediatr Neurol. 1995 Jul;13(1):65-8 [7575853.001]
  • [Cites] Acta Neuropathol. 1996;91(6):578-86 [8781656.001]
  • [Cites] J Korean Med Sci. 2002 Oct;17(5):723-6 [12378033.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1993;422(1):81-5 [7679853.001]
  • [Cites] J Neurooncol. 2003 Feb;61(3):219-25 [12675315.001]
  • [Cites] Pediatr Radiol. 2003 Apr;33(4):275-7 [12709762.001]
  • [Cites] J Neurosurg. 1996 Jul;85(1):56-65 [8683283.001]
  • [Cites] Med Pediatr Oncol. 1999 May;32(5):389-91 [10219345.001]
  • [Cites] Cancer. 1991 Apr 15;67(8):2058-61 [2004323.001]
  • [Cites] Pediatr Neurosurg. 1995;22(4):214-22 [7619723.001]
  • [Cites] Ultrastruct Pathol. 1994 Jan-Apr;18(1-2):23-8 [8191632.001]
  • [Cites] J Neurooncol. 2001 Aug;54(1):53-6 [11763423.001]
  • [Cites] Neurology. 1991 Nov;41(11):1847-8 [1944923.001]
  • [Cites] Clin Neuropathol. 1991 Jan-Feb;10(1):1-10 [2015720.001]
  • [Cites] Childs Nerv Syst. 1987;3(6):379-81 [3450389.001]
  • [Cites] J Pediatr Hematol Oncol. 1995 Feb;17(1):71-5 [7743242.001]
  • [Cites] J Comput Assist Tomogr. 1990 May-Jun;14 (3):461-3 [2335617.001]
  • [Cites] Pediatr Neurosurg. 1994;21(4):232-6 [7865408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13796-800 [11095756.001]
  • [Cites] Pediatr Pathol. 1989;9(3):307-19 [2546137.001]
  • [Cites] Childs Nerv Syst. 2003 Apr;19(4):244-8 [12682757.001]
  • [Cites] Hum Pathol. 1987 Apr;18(4):332-7 [3030922.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1083-92 [9737241.001]
  • [Cites] Postgrad Med J. 1998 Jun;74(872):369-70 [9799897.001]
  • [Cites] Childs Nerv Syst. 2000 Apr;16(4):228-34 [10855521.001]
  • [Cites] Med Pediatr Oncol. 1992;20(3):258 [1637409.001]
  • (PMID = 15803379.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 37
  •  go-up   go-down


14. Roland JT Jr, Cosetti M, Liebman T, Waltzman S, Allen JC: Cochlear implantation following treatment for medulloblastoma. Laryngoscope; 2010 Jan;120(1):139-43
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cochlear implantation following treatment for medulloblastoma.
  • OBJECTIVES/HYPOTHESIS: Medulloblastoma is the most common pediatric malignant tumor of the central nervous system in children.
  • Treatment includes surgical excision, external beam radiation, and multiagent chemotherapy.
  • Otologic sequelae are common and may result from radiation and/or chemotherapy.
  • Profound sensorineural hearing loss (SNHL) is a known complication of neuro-oncologic treatment and may render these patients eligible for cochlear implantation (CI).
  • Issues of CI in this population, including diagnosis, treatment of preoperative middle ear disease, operative and postoperative course, performance data, and long-term tumor surveillance are highlighted and reviewed.
  • METHODS: Three patients treated for pediatric medulloblastoma with surgical resection, postoperative hyperfractioned craniospinal radiotherapy, and multiagent adjuvant chemotherapy who underwent cochlear implantation were identified.
  • Details of neuro-oncologic treatment and associated otologic complications are presented and analyzed.
  • Primary outcome assessment includes treatment of middle ear pathology, perioperative cochlear implant course, and postimplantation performance data.
  • RESULTS: Each patient required surgical treatment of chronic ear disease 4 to 16 years after chemoradiation.
  • All progressed to profound SNHL and were implanted 8 to 17 years post-neuro-oncologic treatment.
  • One patient developed postoperative wound dehiscence requiring operative closure.
  • CONCLUSIONS: Patients treated for pediatric medulloblastoma develop otologic sequelae, including profound SNHL, and may require cochlear implantation.
  • [MeSH-major] Brain Neoplasms / therapy. Cochlear Implantation. Hearing Loss, Sensorineural / surgery. Medulloblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Combined Modality Therapy. Humans. Retrospective Studies. Treatment Outcome


15. Büyükpamukçu M, Varan A, Yazici N, Akalan N, Söylemezoğlu F, Zorlu F, Akyüz C, Kutluk MT: Second malignant neoplasms following the treatment of brain tumors in children. J Child Neurol; 2006 May;21(5):433-6
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second malignant neoplasms following the treatment of brain tumors in children.
  • We investigated retrospectively 992 children with central nervous system tumors who were treated at our center between 1970 and 2004.
  • All of the patients were treated by surgery, chemotherapy, and/or radiotherapy.
  • Six patients developed second malignant neoplasms, and their clinical and histopathologic characteristics are reviewed in this article.
  • The second malignant neoplasms were diagnosed as non-Hodgkin lymphoma, myelodysplastic syndrome, basal cell carcinoma, malignant melanoma, Kaposi sarcoma, and high-grade neuroectodermal tumor.
  • The median latency time was 3.03 years (range 0.39-22.93 years).
  • The outcome varied according to the histopathologic type of the second tumor.
  • The patients who developed non-Hodgkin lymphoma and myelodysplastic syndrome died of progressive disease.
  • The patients with second skin neoplasms are alive as of the time of this writing.
  • The patient with Kaposi sarcoma developed one of the rare reported second malignant neoplasms following a primary brain tumor in childhood.
  • A wide spectrum of second malignant neoplasms was detected after treatment of primary brain tumors with surgery, radiotherapy, and chemotherapy.
  • Long-term follow-up is therefore necessary for the child who has survived a primary central nervous system tumor.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Glioma / pathology. Glioma / therapy. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Male. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16901454.001).
  • [ISSN] 0883-0738
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Chen ML, McComb JG, Krieger MD: Atypical teratoid/rhabdoid tumors of the central nervous system: management and outcomes. Neurosurg Focus; 2005 Jun 15;18(6A):E8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical teratoid/rhabdoid tumors of the central nervous system: management and outcomes.
  • OBJECT: Atypical teratoid/rhabdoid tumors (ATRTs) represent a relatively newly categorized neoplastic entity.
  • They commonly present in childhood, and have a rapidly progressive clinical course with a survival time of less than 1 year.
  • Treatment regimens have been nonuniform.
  • In this retrospective review of patients with ATRTs who were treated at the authors' institution according to a uniform protocol, the goal was to assess the efficacy of the treatment and its outcome.
  • Tumor location was cortical in four patients, in the pineal region in four, in the posterior fossa in two, and spinal in one.
  • In one patient disseminated disease was revealed on the initial imaging study; seven patients had disseminated tumor subsequently.
  • Treatment consisted of chemotherapy in 11 patients, chemotherapy and local radiation in five, and chemotherapy and craniospinal radiation in three.
  • The mean time to death was 24 months, and ranged from 2 to 67 months.
  • The median time to progression was 3.5 months.
  • CONCLUSIONS: Atypical teratoid/rhabdoid tumors are malignant lesions with rapid progression.
  • Further study is necessary to determine the efficacy of therapy.
  • [MeSH-major] Central Nervous System Neoplasms / therapy. Rhabdoid Tumor / therapy. Teratoma / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Magnetic Resonance Imaging / methods. Male. Retrospective Studies. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16048294.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Moftakhar P, Fan X, Hurvitz CH, Black KL, Danielpour M: Long-term survival in a child with a central nervous system medulloepithelioma. J Neurosurg Pediatr; 2008 Nov;2(5):339-45
MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival in a child with a central nervous system medulloepithelioma.
  • Central nervous system medulloepitheliomas are extremely rare and malignant (World Health Organization Grade IV) primitive neuroectodermal tumors (PNETs) that arise in childhood.
  • Unlike other PNETs, medulloepitheliomas have a dismal prognosis, with only 2 reported cases in the literature in which the patient survived beyond 5 years after treatment.
  • A review of all the published cases of medulloepithelioma is also presented, and alternative treatment strategies for PNET tumors, including high-dose chemotherapy with stem-cell rescue, are discussed.
  • [MeSH-major] Brain Neoplasms / pathology. Brain Neoplasms / therapy. Neuroectodermal Tumors, Primitive / pathology. Neuroectodermal Tumors, Primitive / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Child. Combined Modality Therapy. Disease-Free Survival. Female. Hematopoietic Stem Cell Transplantation. Humans. Survival Rate

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18976104.001).
  • [ISSN] 1933-0707
  • [Journal-full-title] Journal of neurosurgery. Pediatrics
  • [ISO-abbreviation] J Neurosurg Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 46
  •  go-up   go-down


18. Keir ST, Hausheer F, Lawless AA, Bigner DD, Friedman HS: Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice. Cancer Chemother Pharmacol; 2001 Jul;48(1):83-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic activity of 7-[(2-trimethylsilyl)ethyl)]-20 (S)-camptothecin against central nervous system tumor-derived xenografts in athymic mice.
  • PURPOSE: Camptothecins have emerged as an important new class of antitumor drugs.
  • Camptothecin derivatives such as CPT-11 and topotecan are commercially available and approved for the treatment of colorectal (CPT-11) and ovarian and small-cell lung cancer (topotecan).
  • This study was designed to test the efficacy of karenitecin, a novel highly lipophilic camptothecin derivative, against a panel of human tumor xenografts derived from adult and pediatric central nervous system malignancies growing in athymic nude mice.
  • METHODS: Xenografts evaluated were derived from childhood high-grade gliomas (D-212 MG, D-456 MG), adult high-grade gliomas (D-54 MG, D-245 MG), medulloblastomas (D-341 MED, D-487 MED), and ependymomas (D-528 EP, D-612 EP), as well as sublines with demonstrated resistance to procarbazine (D-245 MG (PR)) and busulfan (D-456 (BR)).
  • CONCLUSION: These preclinical studies confirm that karenitecin is active against human central nervous system xenografts and should undergo clinical evaluation in patients with malignant central nervous system tumors.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy
  • [MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Camptothecin / therapeutic use. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11488529.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 24R60NVC41 / cositecan; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


19. Hurwitz CA, Strauss LC, Kepner J, Kretschmar C, Harris MB, Friedman H, Kun L, Kadota R: Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study. J Pediatr Hematol Oncol; 2001 Jun-Jul;23(5):277-81
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paclitaxel for the treatment of progressive or recurrent childhood brain tumors: a pediatric oncology phase II study.
  • PURPOSE: To assess the efficacy and define the toxicity of paclitaxel given at a dosage of 350 mg/m2 every 3 weeks as a 24-hour continuous infusion to children with recurrent or progressive primary brain tumors.
  • PATIENTS AND METHODS: Seventy-three eligible patients, ages 4 months to 19 years, with progressive or recurrent primary brain tumors were treated according to a Pediatric Oncology Group (POG) phase II protocol with paclitaxel (POG 9330).
  • Tumor histologic strata included: astrocytoma (n = 4), malignant glioma (n = 13), medulloblastoma (n = 16), brain stem glioma (n = 15), ependymoma (n = 13), and miscellaneous histologies (n = 12).
  • All patients had previous histologic confirmation of a primary intracranial or spinal cord tumor with magnetic resonance imaging or computed tomography documentation of unequivocally measurable progressive or recurrent disease.
  • All patients had received previous therapy including surgery, radiation therapy, and/or chemotherapy, but no patient had been previously treated on more than one phase II trial.
  • Patients were allowed to continue therapy for a total of 18 cycles in the absence of progressive disease or unacceptable toxicity.
  • RESULTS: Seventy-five patients were enrolled onto the POG 9330 protocol; two ineligible patients were removed from the study before receiving any therapy.
  • Toxicities included mild nausea, central nervous system toxicity, myelosuppression, and febrile neutropenia, including one septic death.
  • CONCLUSION: Paclitaxel is well tolerated in children with recurrent or progressive brain tumors at this dosage and schedule and may result in short-term disease stabilization in this patient population.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / drug therapy. Paclitaxel / therapeutic use
  • [MeSH-minor] Adolescent. Astrocytoma / drug therapy. Astrocytoma / pathology. Child. Child, Preschool. Dexamethasone / therapeutic use. Disease Progression. Drug Hypersensitivity / prevention & control. Ependymoma / drug therapy. Ependymoma / pathology. Female. Glioma / drug therapy. Glioma / pathology. Humans. Immunosuppressive Agents / therapeutic use. Infant. Infratentorial Neoplasms / drug therapy. Infratentorial Neoplasms / pathology. Infusions, Intravenous. Male. Medulloblastoma / drug therapy. Medulloblastoma / pathology. Nausea / chemically induced. Neoplasm Recurrence, Local. Neutropenia / chemically induced. Remission Induction. Salvage Therapy. Treatment Failure

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11464982.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA03161; United States / NCI NIH HHS / CA / CA07431; United States / NCI NIH HHS / CA / CA15525; etc
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunosuppressive Agents; 7S5I7G3JQL / Dexamethasone; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


20. Gow KW, Lensing S, Hill DA, Krasin MJ, McCarville MB, Rai SN, Zacher M, Spunt SL, Strickland DK, Hudson MM: Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature. J Pediatr Surg; 2003 Nov;38(11):1574-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyroid carcinoma presenting in childhood or after treatment of childhood malignancies: An institutional experience and review of the literature.
  • METHODS: The authors reviewed the medical records of 8 children with PTM and 17 children with STM referred to St Jude Children's Research Hospital between February 1962 and February 2002 for evaluation and treatment of malignant thyroid carcinoma.
  • Seventeen patients had thyroid carcinoma as a second malignant neoplasm after treatment for acute lymphoblastic leukemia (n = 6), Hodgkin's disease (n = 5), central nervous system tumor (n = 2), Wilms' tumor (n = 1), retinoblastoma (n = 1), non-Hodgkin's lymphoma (n = 1), or neuroblastoma (n = 1).
  • Twelve of the 17 patients (70.6%) had received radiation to the thyroid gland during therapy for the primary cancer.
  • At the time of this report, all 17 patients are alive and in continue to be free of disease.
  • CONCLUSIONS: Pediatric thyroid carcinoma is uncommon and responds well to current therapy.
  • Given the limited period of follow-up of our cohort of secondary malignant thyroid tumors that arise after childhood cancer, these lesions appear to have similar presentations and outcomes when compared with primary carcinomas and can therefore be managed in the same manner.
  • [MeSH-major] Adenocarcinoma, Follicular / epidemiology. Carcinoma, Papillary / epidemiology. Neoplasms, Second Primary / epidemiology. Thyroid Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Child. Cohort Studies. Combined Modality Therapy. Female. Humans. Iodine Radioisotopes / therapeutic use. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Neoplasms / drug therapy. Neoplasms / radiotherapy. Neoplasms, Radiation-Induced / epidemiology. Retrospective Studies. Tennessee / epidemiology. Thyroidectomy. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14614703.001).
  • [ISSN] 1531-5037
  • [Journal-full-title] Journal of pediatric surgery
  • [ISO-abbreviation] J. Pediatr. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  • [Number-of-references] 49
  •  go-up   go-down


21. Albert A, Cruz O, Montaner A, Vela A, Badosa J, Castañón M, Morales L: [Congenital solid tumors. A thirteen-year review]. Cir Pediatr; 2004 Jul;17(3):133-6
MedlinePlus Health Information. consumer health - Wilms Tumor.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Congenital solid tumors. A thirteen-year review].
  • Tumors diagnosed during the first month of life are infrequent: 0.5 to 2% of all childhood neoplasms.
  • This is an interesting group of tumors because their type, relative incidence, natural history and response to treatment differ from those seen in older children.
  • AIM: To contribute the experience of our institution in congenital tumors the last 13 years.
  • MATERIAL AND METHODS: The records of all neonates (< 31 days old) diagnosed with solid tumors since January 1990 to December 2002 have been retrospectively reviewed.
  • RESULTS: Twenty-seven neonates have been diagnosed with tumors in the last 13 years.
  • Neuroblastoma was the commonest tumor (10 cases, 37%), of which 4 were stage I, 4 stage IV-S and 2 stage III.
  • There were 8 teratomas (3 sacrocoxigeal, 1 retroperitoneal, 1 in the CNS, 1 orbitary and two oronasal), two hepatic tumors (1 hepatoblastoma, 1 hemangioendothelioma, two CNS tumors, two giant nevus (one on a hamartoma), and one each Wilms tumor, infantile fibrosarcoma and myofibroblastic tumor.
  • Treatment was surgical resection alone in 17 cases (68%) and surgery + chemotherapy in 8 (32%) (5 neuroblastomas, one CNS tumor, one Wilms tumor and one presacral teratoma who developed a yolk sac tumor); 3 patients died (11%): one at surgery, one of tumoural airway obstruction at birth and one with craniopharyngioma.
  • Among the 14 tumors that were initially not malignant, two can be locally agressive, one was an immature teratoma, the giant nevus with hamartoma developed in situ melanoma, the other nevus had meningeal melanosis with hydrocephalus, and one mature presacral teratoma developed a yolk sac tumor.
  • CONCLUSIONS: Diagnosis of congenital tumors is performed earlier in recent years due to the wide use of prenatal ultrasound.
  • Their natural history is more benign than in other age groups, except for CNS tumors and very large or obstructing tumors.
  • Complete surgical excision is the treatment of choice, most cases not need adjuvant chemotherapy.
  • [MeSH-major] Central Nervous System Neoplasms / congenital. Kidney Neoplasms / congenital. Liver Neoplasms / congenital. Neuroblastoma / congenital. Skin Neoplasms / congenital. Soft Tissue Neoplasms / congenital. Teratoma / congenital. Wilms Tumor / congenital
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Infant, Newborn. Male. Neoplasm Recurrence, Local. Postoperative Complications. Pregnancy. Prenatal Diagnosis. Time Factors

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15503950.001).
  • [ISSN] 0214-1221
  • [Journal-full-title] Cirugía pediátrica : organo oficial de la Sociedad Española de Cirugía Pediátrica
  • [ISO-abbreviation] Cir Pediatr
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


22. Cavazos CM, Keir ST, Yoshinari T, Bigner DD, Friedman HS: Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts. Cancer Chemother Pharmacol; 2001 Sep;48(3):250-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic activity of the topoisomerase I inhibitor J-107088 [6-N-(1-hydroxymethyla-2-hydroxyl) ethylamino-12,13-dihydro-13-(beta-D-glucopyranosyl) -5H-indolo[2,3-a]-pyrrolo[3,4-c]-carbazole-5,7(6H)-dione]] against pediatric and adult central nervous system tumor xenografts.
  • PURPOSE: The in vivo antitumor activity of a novel topoisomerase I inhibitor, J-107088, was tested in athymic nude mice bearing subcutaneous or intracranial pediatric and adult malignant CNS tumor-derived xenografts.
  • The xenografts evaluated were derived from a childhood glioblastoma multiforme (D-456 MG), a childhood medulloblastoma (D-341 MED), an adult anaplastic astrocytoma (D-54 MG), an adult glioblastoma multiforme (D-245 MG), and a procarbazine-resistant subline of D-245 MG [D-245 MG (PR)].
  • Growth delays ranged from 7.6 days with D-245 MG to 62.1 days with D-456 MG (P < 0.001).
  • CONCLUSION: These results indicate that J-107088 may be active in the treatment of childhood and adult malignant brain tumors and provide the rationale for initiation of clinical trials with this agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain Neoplasms / drug therapy. Carbazoles / therapeutic use. Enzyme Inhibitors / therapeutic use. Glioma / drug therapy. Glucosides / therapeutic use. Indoles. Topoisomerase I Inhibitors
  • [MeSH-minor] Adult. Animals. Child. Female. Humans. Injections, Intraperitoneal. Injections, Subcutaneous. Male. Mice. Mice, Nude. Neoplasm Transplantation. Survival Rate. Transplantation, Heterologous. Treatment Outcome. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11592348.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / 2RO1-NS30245-12; United States / NINDS NIH HHS / NS / 5P50-NS-20023-17; United States / NCI NIH HHS / CA / CA11898; etc
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Enzyme Inhibitors; 0 / Glucosides; 0 / Indoles; 0 / Topoisomerase I Inhibitors; 1V8X590XDP / edotecarin
  •  go-up   go-down


23. Mulhern RK, Khan RB, Kaplan S, Helton S, Christensen R, Bonner M, Brown R, Xiong X, Wu S, Gururangan S, Reddick WE: Short-term efficacy of methylphenidate: a randomized, double-blind, placebo-controlled trial among survivors of childhood cancer. J Clin Oncol; 2004 Dec 1;22(23):4795-803
Hazardous Substances Data Bank. METHYLPHENIDATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short-term efficacy of methylphenidate: a randomized, double-blind, placebo-controlled trial among survivors of childhood cancer.
  • PURPOSE: Children surviving acute lymphoblastic leukemia (ALL) and malignant brain tumors (BTs) have a higher incidence of attention and learning problems in school than do their healthy peers.
  • The primary end points were weekly teacher and parent reports on the Conners' Rating Scales and Social Skills Rating System.
  • RESULTS: Compared to placebo, significant improvement with MPH was reported by teachers and parents on the Conners' Rating Scales and by teachers on the Social Skills Rating System.
  • CONCLUSION: Treatment with MPH can at least temporarily reduce some attentional and social deficits among survivors of childhood ALL and BT.
  • [MeSH-major] Attention Deficit Disorder with Hyperactivity / drug therapy. Brain Neoplasms / complications. Central Nervous System Stimulants / administration & dosage. Cognition Disorders / drug therapy. Methylphenidate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Child. Cross-Over Studies. Dose-Response Relationship, Drug. Double-Blind Method. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Probability. Reference Values. Risk Assessment. Severity of Illness Index. Survivors. Treatment Outcome

  • Genetic Alliance. consumer health - Childhood Cancer.
  • MedlinePlus Health Information. consumer health - Attention Deficit Hyperactivity Disorder.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Childhood Brain Tumors.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Clin Oncol. 2005 Jan 1;23(1):248
  • (PMID = 15570081.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA21765; United States / NCI NIH HHS / CA / R01 CA78957; United States / NCI NIH HHS / CA / U01 CA81445
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 207ZZ9QZ49 / Methylphenidate
  •  go-up   go-down


24. Vázquez E, Castellote A, Piqueras J, Ortuno P, Sánchez-Toledo J, Nogués P, Lucaya J: Second malignancies in pediatric patients: imaging findings and differential diagnosis. Radiographics; 2003 Sep-Oct;23(5):1155-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Second malignancies in pediatric patients: imaging findings and differential diagnosis.
  • Therapeutic advances in the treatment of pediatric neoplasms have improved the prognosis but have also increased the risk of developing rare second malignant neoplasms (SMNs).
  • Primary neoplasms that are often associated with SMNs include lymphoma, retinoblastoma, medulloblastoma, neuroblastoma, and leukemia.
  • The most common SMNs are central nervous system (CNS) tumors, sarcomas, thyroid and parotid gland carcinomas, and leukemia, particularly acute myeloblastic leukemia.
  • Genetic predisposition, chemotherapy, and especially radiation therapy are implicated as pathogenic factors in SMN.
  • All survivors of childhood cancer should have lifelong follow-up, preferably with magnetic resonance imaging, which does not require ionizing radiation and provides greater anatomic detail and resolution in the head and neck region and the CNS.
  • Treatment protocols should be modified to reduce the risk for SMN without compromising the effectiveness of initial therapy.
  • Clinicians should individualize treatment for patients who are genetically predisposed to SMN.
  • In addition, radiologists should be familiar with the long-term consequences of antineoplastic therapy to facilitate diagnosis and anticipate adverse outcomes.
  • [MeSH-major] Neoplasms, Second Primary / radiography

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright RSNA, 2003
  • (PMID = 12975507.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 52
  •  go-up   go-down


25. Papaefthymiou MA, Giaginis CT, Theocharis SE: DNA repair alterations in common pediatric malignancies. Med Sci Monit; 2008 Jan;14(1):RA8-15
MedlinePlus Health Information. consumer health - Cancer in Children.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA repair alterations in common pediatric malignancies.
  • However, our knowledge on DNA repair defects, both in germline and somatic mutations, and their relationship with childhood malignancies remains incomplete.
  • Mutations, gene deletions, and inversions in various DNA repair genes have been reported and special attention has recently been focused on the interaction between these abnormalities and malignant transformation in childhood.
  • The purpose of this review is to summarize the existing clinical information concerning components of the DNA repair systems and their influence on the development of the most common pediatric malignancies, including leukemia, tumors of the central nervous system, rhabdomyosarcoma, and retinoblastoma.
  • Such information could possibly explain the response or resistance to chemotherapy and the possible risk of relapse in childhood malignancies presenting specific DNA repair defects.
  • Additionally, these data could be beneficial for the development of novel therapeutic strategies.
  • [MeSH-major] DNA Repair / genetics. Neoplasms / genetics
  • [MeSH-minor] Central Nervous System Neoplasms / genetics. Central Nervous System Neoplasms / metabolism. Child. DNA Damage. DNA Mismatch Repair. Humans. Leukemia / genetics. Leukemia / metabolism. Mutation. Polymorphism, Genetic. Retinal Neoplasms / genetics. Retinal Neoplasms / metabolism. Retinoblastoma / genetics. Retinoblastoma / metabolism. Rhabdomyosarcoma / genetics. Rhabdomyosarcoma / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18160950.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 44
  •  go-up   go-down


26. Schiavetti A, Clerico A, De Pasquale MD, Bernardini L, Moleti ML: Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2003 Jul;25(7):562-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medulloblastoma as a secondary malignancy after radiotherapy-free treatment for acute lymphoblastic leukemia.
  • Malignant brain tumors have been reported to occur in survivors of childhood acute lymphoblastic leukemia (ALL) more frequently than in the noncancer control population.
  • The strongest risk factor seems to be cranial radiotherapy, used as central nervous system (CNS) prophylaxis.
  • We report the case of a 9-year-old girl affected with metastatic medulloblastoma that developed 6 years after a diagnosis of acute lymphoblastic leukemia.
  • CNS prophylaxis for ALL consisted of intrathecal methotrexate plus cytarabine (20 administrations) and 4 courses of high-dose methotrexate (5g/m2).
  • The child, in first complete remission, was well until the occurrence of a second tumor.
  • She was treated for medulloblastoma with craniospinal radiotherapy and chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebellar Neoplasms / radiotherapy. Medulloblastoma / radiotherapy. Neoplasms, Second Primary / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Female. Humans. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Medulloblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12847325.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


27. Marchetti D, Mrak RE, Paulsen DD, Sinnappah-Kang ND: Neurotrophin receptors and heparanase: a functional axis in human medulloblastoma invasion. J Exp Clin Cancer Res; 2007 Mar;26(1):5-23
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Medulloblastoma (MB) is the most common malignant brain tumor of childhood.
  • Although modern therapy has produced five-year survival rates as high as 70% for some MB patients, this resulted in significant long-term treatment-related morbidity.
  • Neurotrophins (NT) comprise a family of structurally and functionally related neurotrophic factors that are critical for central nervous system (CNS) development with nerve growth factor (NGF) being the prototypic NT.
  • NT acts through two groups of structurally unrelated neurotrophin receptors (NTR): a family of receptor tyrosine kinases (Trks, mainly TrkA, TrkB, and TrkC) and a tumor necrosis factor receptor (TNFR)-like molecule called p75NTR TrkC expression is a good prognostic indicator for MB.
  • Importantly, little is known about the biological functions of p75 in primitive neuroectodermal tumors such as MB.
  • In contrast, NT-regulated heparanase (HPSE) is a unique extracellular matrix-degrading enzyme known to be associated with tumor progression in a wide variety of cancers.
  • We provide evidence of a differential expression of HPSE in newly-developed medulloblastoma cell lines.
  • Finally, by using antibodies specific to TrkC and immunohistochemistry (IHC) we prove that IHC scores reveal a significant expression of HPSE in 76% of MB tissues from children aged 3 years and older.
  • Taken together, our data provide evidence that HPSE functionality, in a context linked to TrkC and p75NTR activation, may play critical roles in medulloblastoma tumor invasion and progression.
  • [MeSH-major] Cerebellar Neoplasms / metabolism. Glucuronidase / metabolism. Medulloblastoma / metabolism. Meningeal Neoplasms / metabolism. Receptors, Nerve Growth Factor / metabolism
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Infant. Male. NF-kappa B / metabolism. Neoplasm Invasiveness. Nerve Tissue Proteins / metabolism. Neurotrophin 3 / metabolism. Neurotrophin 3 / pharmacology. Phosphorylation. Prognosis. Receptor, trkC / metabolism

  • Genetic Alliance. consumer health - Medulloblastoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17550129.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA086832; United States / NCI NIH HHS / CA / CA103955
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / NGFR protein, human; 0 / Nerve Tissue Proteins; 0 / Neurotrophin 3; 0 / Receptors, Nerve Growth Factor; EC 2.7.10.1 / Receptor, trkC; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
  •  go-up   go-down






Advertisement